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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since increased opiate production in obesity has been reported, the effects of naloxone in obese subjects were studied in order to ascertain whether endogenous opioid peptides play a role in the abundant insulin secretion of obesity. The results obtained showed that intravenous administration of naloxone considerably reduced insulin of obese subjects to a mixed meal, whereas it did not modify the blood insulin response to arginine or glucose infusion. Glucagon secretion to ingestion of a mixed meal and to arginine infusion was not modified by the opioid receptor blocking agent. This study seems to indicate that hyperproduction of endogenous opioid peptides in obesity increases insulin secretion stimulated by food intake, whereas it does not appreciably affect insulin production stimulated by circulating glucose or aminoacids.
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PMID:Possible involvement of endogenous opioids in beta-cell hyperresponsiveness in human obesity. 252 25

Fifty obese (BMI = 40.1 +/- 1.5) subjects (21 men and 21 women; average age 38.6 +/- 3.8 years) were prescribed a 600 cal/day diet (carbohydrates 30 g, proteins 60 g, lipids 10 g). Thirty patients were also given benfluorex (three tablets/day) for six months (Group A), whereas the other 20 patients (Group B) were treated with the dietary measures only. Apart from grade II and III obesity, several patients suffered from dyslipidaemia (Group A: n = 10; Group B: n = 7), non-insulin-dependent diabetes mellitus (NIDDM) (Group A: n = 4; Group B: n = 3) or IGT (Group A: n = 8; Group B: n = 6). The usual blood and biochemical tests and clinical examinations were carried out on Days 0, 90 and 180, together with the OGTT and glucagon test to determine blood glucose levels, IRI and CPR. There was no statistical difference between the weight loss of Group A and that of Group B. In Group A there was a statistically significant reduction (p less than 0.001) in total cholesterol, triglycerides, total/HDL-cholesterol and beta/alpha-lipoproteins and a significant increase in HDL-cholesterol and alpha-lipoproteins (p less than 0.001), whereas in Group B only a significant reduction in triglycerides (p less than 0.001) was observed. In NIDDM patients treated with benfluorex, normalisation of basal blood glucose levels was accompanied by an improvement in the OGTT blood glucose curve which was statistically significant relative to Group B. Benfluorex was well tolerated by all patients and no adverse event was reported.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of benfluorex in obese patients with metabolic disorders. 259 99

The gastrointestinal hormone, gastric inhibitory polypeptide (GIP), has been isolated and characterized because of its enterogastrone-type effects. It is also named glucose-dependent insulinotropic polypeptide and is actually considered to be the main incretin factor of the entero-insular axis. Besides these well-described effects on gastric secretion and pancreatic beta cells, it also has direct metabolic effects on other tissues and organs, such as adipose tissue, liver, muscle, gastrointestinal tract and brain. In adipose tissue it is involved in the activation and regulation of lipoprotein lipase (LPL); it also inhibits glucagon-induced lipolysis and potentiates the effect of insulin on incorporation of fatty acids into triglycerides. It may play a role in the development of obesity because of the hypersensitivity of adipose tissue of obese animals to some of these actions. In the liver it does not modify insulin extraction, and its incretin effects are due only to the stimulation of insulin secretion and synthesis. It reduces hepatic glucose output and inhibits glucagon-stimulated glycogenolysis. It might increase glucose utilization in peripheral tissues such as muscle. GIP also has an effect on the volume and/or electrolyte composition of intestinal secretion and saliva. The functional importance of its effect on the hormones of the anterior pituitary lobe remains to be established, as it has never been detected in the brain. Its links with insulin are very close and the presence of insulin is sometimes necessary for the greater efficiency of both hormones. GIP can be considered as a true metabolic hormone, with most of its functions tending to increase anabolism.
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PMID:Gastric inhibitory polypeptide: a gut hormone with anabolic functions. 266 79

We put 12 obese subjects on a very-low-calorie diet (VLCD) and observed how their weight loss affected their glucose tolerance. Seven had non-insulin-dependent diabetes and five did not. They consumed 1000 kcal/day for at least 1 week, then 420 kcal/day for 4 weeks, and 1000 kcal/day thereafter. VLCD improved glucose tolerance and insulin response to a glucose load in the diabetics and did not affect these parameters in the non-diabetics. It did not change insulin responsiveness to intravenous glucagon in either group. Both groups showed improved insulin resistance, as measured by an insulin suppression test. Regression analysis showed that insulin resistance correlates well with obesity and glycemic control. Weight reduction did not change hepatic insulin extraction. Thus, the improvement in glucose tolerance by some of the diabetics seems to have arisen from improvements in their insulin resistance and insulin response to a glucose load. Insulin resistance improved because of weight reduction and subsequent improvements in glycemic control.
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PMID:Effects of very-low-calorie diet weight reduction on glucose tolerance, insulin secretion, and insulin resistance in obese non-insulin-dependent diabetics. 266 69

The metabolic characteristics of nine postobese and six lean control male individuals were investigated to identify factors potentially associated with the predisposition to become obese. The postobese subjects had been maintaining their body weight stable for at least six months following a 24.8 kg mean weight loss. Body weight, fat mass and fat-free mass were comparable to values of the control subjects. Data obtained in postobese and control subjects were also compared to those of seven obese male individuals whose mean body weight was comparable to the body weight of postobese subjects before they initiated their weight-reducing program. Resting metabolic rate (RMR) was significantly higher (P less than 0.05) in the obese than in the two other groups. Thermic effect of food and participation in physical activities were similar in the three groups of subjects. Daily energy intake tended to be higher in control subjects but not to a statistically significant extent. However, energy intake above RMR was statistically higher in control subjects than in the two other groups. As expected, fasting and postprandial plasma glucose and insulin were substantially higher in obese than in postobese and control subjects. Moreover, fasting and postprandial hyperglucagonemia was observed in both obese and postobese subjects, suggesting that weight loss did not normalize plasma glucagon levels as was the case for glucose and insulin. From an energetic standpoint, results of the present study suggest that people predisposed to obesity may be characterized by reduced energy needs over resting metabolic rate, a phenomenon that would not be explained by a reduced physical activity level.
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PMID:Metabolic characteristics of postobese individuals. 267 Jul 93

A standard oral glucose tolerance test was performed in 86 healthy premenopausal obese Arab women (BMI greater than or equal to 30) Glucose, insulin and glucagon were measured at 0, 30, 60, 90 and 120 min. Sex hormone binding globulin (SHBG), plasma lipids and uric acid were also estimated. Waist-hip circumference ratio (WHR) had significant positive correlation with age, triglycerides (TG), uric acid, fasting and 120 min glucose, and 120 min insulin and significant negative correlation with SHBG. Body mass index (BMI) had significant correlation with uric acid, fasting and 120 min insulin, and significant negative correlation with high density lipoprotein cholesterol (HDL Chol). When separated in two subgroups, with WHR greater than 0.80 (41), and less than or equal to 0.80 (45 cases), plasma glucose was in the diabetic range in seven; and impaired glucose tolerance (IGT) in 11 women in the former subgroup. Only three with IGT but no diabetics, were in lower WHR subgroup. WHR in diabetics (0.93), and in IGT cases (0.90) was significantly higher than in other women (0.80). Fasting insulin was not different, but at 90 and 120 min, insulin was higher in the high WHR subgroup who had also higher fasting, 90 and 120 min glucose. Glucagon level, though slightly higher in the higher (WHR) subgroup, may indicate relative hyperglucagonaemia because of the associated significantly higher glucose. Compared with age matched non-obese controls, obese women in both subgroups had significantly higher insulin, uric acid and significantly lower HDL Chol and lower glucagon (insignificant). Obese women in the higher WHR subgroup (greater than 0.80) had also significantly higher systolic blood pressure, TG and lower SHBG.
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PMID:Pattern of obesity and insulin, glucagon, sex hormone binding globulin and lipids in obese Arab women. 269 44

To investigate glucagon (IRG) and insulin (IRI) responses to alanine infusion in obesity and to assess the effect of body weight reduction with respect to hormonal balance, we compared six obese subjects with nine normal weight controls. None of the subjects were diabetic by OGTT criteria. Plasma IRI and IRG were measured following IV alanine at a rate of 0.1 g/kg over a period of 2 min. Our obese subjects had an increase in IRG response to alanine, which was due to decreased suppression of alpha-cell function due to insulin resistance. Weight reduction via calorie restriction reduced insulin demand, resulting in reduced plasma IRI by restoring beta-cell function, and the IRG response was paradoxically decreased as compared with that before weight loss. It is conceivable that improvements in insulin sensitivity after body weight reduction may re-establish the normalization of pancreatic beta-cell function and the insulin-induced inhibition of IRG secretion. Our obese subjects were characterized by decreased IRG secretion which was reflected in a change in body weight reduction.
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PMID:Plasma glucagon response to intravenous alanine in obese and non-obese subjects. 269 21

To elucidate if the presence of fatty liver and hypertriglyceridemia (HTG) influences pancreatic A-cell function in obesity, basal and arginine-stimulated glucagon (IRG) secretions were studied in 7 normal subjects and in 28 moderately obese patients (OB) with normal glucose tolerance. The patients were divided into 4 groups, based on the presence of fatty liver and/or HTG. BMI was similar in all four obese groups. Basal IRG, as well as the sum of secretory response to arginine, namely sigma IRG values, were significantly (p less than 0.01) higher in the OB subgroup having both fatty liver and HTG than in the other three groups; these values were similar in subgroups of OB without fatty liver, and showed no significant difference from the normals. Basal and sigma IRG values in all OB correlated well with the degree of fatty liver and HTG, demonstrating that by stepwise analysis the effects of fatty liver and HTG were independent for basal and sigma IRG values. These results suggest that the combination of fatty liver and HTG may serve as a good predictor of hyperglucagonemia in simple obesity, and, hence, metabolic heterogeneity among obese patients should be considered in evaluating A-cell function.
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PMID:Elevated pancreatic glucagon in moderately obese patients: relationship of fatty liver and hypertriglyceridemia. 273 44

Pancreatic islet peptides, as well as other gastrointestinal hormones, have been implicated in both the pathogenesis of obesity and the etiology of associated metabolic derangements. This study evaluated the pancreatic islet and gastrointestinal (GI) hormone response to oral glucose in 20 morbidly obese (151% above ideal body weight) patients. Glucose intolerance, hyperinsulinism, and exaggerated gastric inhibitory polypeptide (GIP) release occurred following glucose ingestion. Significant release of PP occurred in 14 patients, while only six patients had release of somatostatin. No significant changes in plasma concentrations of glucagon occurred. Since GIP is insulinotropic in the presence of hyperglycemia, the hyperinsulinism of morbid obesity may be secondary to the abnormally high glucose-stimulated GIP levels in these patients. Failure of glucagon suppression in response to oral glucose many contribute to the hyperglycemia noted. Somatostatin and pancreatic polypeptide may be responsible for some of the metabolic derangements of morbid obesity.
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PMID:Pancreatic islet hormone response to oral glucose in morbidly obese patients. 286 Aug 76

Increased pancreatic somatostatin (somatotrophin release inhibiting factor (SRIF) has been found in hypothyroid rats. Therefore, we wanted to investigate plasma SRIF in patients with hypo- and hyperthyroidism. Two groups of patients, 7 cases with autoimmune hypothyroidism, 31-75 years old, and 7 cases with Graves' disease, 19-43 years old, were compared with regard to plasma SRIF before, during and after an arginine infusion (0.5 g/kg/20 min). None of the patients suffered from diabetes mellitus or obesity. Plasma SRIF was higher in the hypothyroid patients (mean basal value 21.5 +/- 3.9, peak value 28.7 +/- 5.1 pmol/l) compared with the hyperthyroid group (mean basal value 11.6 +/- 3.3, peak value 16.2 +/- 4.0 pmol/l). The hypothyroid group also had significantly higher serum insulin values during arginine stimulation. No difference was found in plasma glucagon, serum growth hormone (GH) or blood glucose. In conclusion, plasma SRIF is elevated in primary hypothyroidism compared with hyperthyroidism. The reason for this finding is uncertain, but a reduced SRIF clearance is a possible explanation. The association of our findings with the reduced glucose tolerance in hyperthyroidism is discussed.
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PMID:Plasma somatostatin is elevated in primary hypothyroidism compared with hyperthyroidism. 287 May 98


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